Plumbagin has an inhibitory effect on the growth of TSCC PDX model and it enhances the anticancer efficacy of cisplatin.

BACKGROUND: Head and neck squamous cell carcinomas are the sixth most common malignant tumors worldwide. Tongue squamous cell carcinoma is a common malignant tumor of this type, and it is associated with poor prognosis, a high rate of recurrence and a low survival rate. Plumbagin is derived from Plumbago zeylanica L, several studies report that plumbagin could inhibit cell, tumor metastasis, induce apoptosis in various cancer cells. Patient-derived xenograft (PDX) model can maintain the heterogeneity and microenvironment of human tumors, is a powerful research tool for developing potentially effective therapies for TSCC. METHODS: Tumor tissues obtained from TSCC patients were implanted into immunodeficient mice to establish TSCC PDX models. Subsequently, the PDX models were used to evaluate the anti-tumor effects of plumbagin on TSCC. Furthermore, we conducted next-generation sequencing (NGS) and explored the mRNA expression profiles between the treatment and control groups. We selected eight mRNAs related to the characteristics and prognosis of TSCC patients for further analysis. RESULTS: Plumbagin could inhibit the growth of TSCC PDX models and inhibit expression of Akt/mTOR pathway. In addition, plumbagin was shown to increase drug sensitivity to cisplatin. The eight mRNAs selected for further analysis, AXL, SCG5, VOPP1, DCBLD2 and DRAM1 are cancer-promoting genes, DUSP1, AQP5 and BLNK are cancer suppressor genes. And they were related to the diagnosis, growth, prognosis, and immune cell infiltration in TSCC patients. CONCLUSION: Plumbagin exhibits an inhibitory effect on the growth of the PDX model of TSCC. Moreover, plumbagin enhances the inhibitory effects of cisplatin.

Corrigendum: MXene nanomaterials in biomedicine: a bibliometric perspective.

[This corrects the article DOI: 10.3389/fbioe.2023.1184275.].

MXene nanomaterials in biomedicine: A bibliometric perspective.

Purpose: MXene is two-dimensional (2D) nanomaterials that comprise transition metal carbides, nitrides, and carbonitrides. Their unique nanostructure attributes it a special role in medical applications. However, bibliometric studies have not been conducted in this field. Therefore, the aim of the present study was to conduct a bibliometric analysis to evaluate the global scientific output of MXene in biomedical research, explore the current situation of this field in the past years and predicte its research hotpots. Methods: We utilized visual analysis softwares Citespace and Bibliometrix to analyze all relevant documents published in the period of 2011-2022. The bibliometric records were obtained from the Web of Science Core Collection. Results: A total of 1,489 publications were analyzed in this study. We observed that China is the country with the largest number of publications, with Sichuan University being the institution with the highest number of publications in this field. The most publications on MXene medicine research in the past year were found primarily in journals about Chemistry/Materials/Physics. Moreover, ACS Applied Materials and Interfaces was found to be the most productive journal in this field. Co-cited references and keyword cluster analysis revealed that #antibacterial# and #photothermal therapy# are the research focus keyword and burst detection suggested that driven wearable electronics were newly-emergent research hot spots. Conclusion: Our bibliometric analysis indicates that research on MXene medical application remains an active field of study. At present, the research focus is on the application of MXene in the field of antibacterial taking advantage of its photothermal properties. In the future, wearable electronics is the research direction of MXene medical application.

Construction of prognostic signature of patients with oral squamous cell carcinoma based on pyroptosis-related long non-coding RNAs.

Background and objective: Oral squamous cell carcinoma (OSCC) is the most common malignant tumor in the head and neck, and its morbidity and mortality are increasing year by year. Changes in key genes are thought to be closely related to the occurrence and development of OSCC. Pyroptosis is an inflammatory form of programmed cell death that has been implicated in malignancies and inflammatory diseases. Changes in the expression of long noncoding RNAs may also affect tumorigenesis and progression. In this study, our main objective was to evaluate the association between pyroptosis-related lncRNAs and prognosis in patients with OSCC. Methods: The RNA-seq data and clinicopathological data of OSCC patients are from The Cancer Genome Atlas database. The pyroptosis gene set is obtained from Gene Set Enrichment Analysis database. Univariate COX, Lasso and multivariate COX regression analyses were used for the construction of risk prognostic models of OSCC, eight lncRNAs were incorporated into prognostic models. The Kaplan-Meier method and log-rank test were used to evaluate the differences of overall survival between patients in high-risk and low-risk groups. The reliability of predictions across the dataset was analyzed by receiver operating characteristic (ROC) curves. The immune signature score was calculated using the single-sample gene set enrichment analysis. Results: Eight pyroptosis-related lncRNAs were used to construct prognostic signature of OSCC, including AC136475.2, AC024075.2, JPX, ZFAS1, TNFRSF10A-AS1, LINC00847, AC099850.3 and IER3-AS1. According to this prognostic signature, patients with OSCC were divided into high-risk and low-risk groups. Kaplan-Meier survival analysis showed that the survival rate of the high-risk group was significantly lower than the low-risk group. ROC area for risk score was 0.716, and ROC area of the 8 lncRNAs are all between 0.5 and 1, implied that these lncRNAs had high accuracy in predicting the prognosis of OSCC patients. Immune Infiltration findings suggested that these lncRNAs affected immune responses in the microenvironment of OSCC. Conclusion: The prognostic signature based on pyroptosis-related lncRNAs potentially serves as an independent prognostic indicator for OSCC patients. And this signature facilitates research on targeted diagnosis and treatment of patients diagnosed with OSCC.

Establishment and Identification of Patient-Derived Xenograft Model for Oral Squamous Cell Carcinoma.

Oral squamous cell carcinoma is the most common head and neck malignancy with high morbidity and mortality. Currently, platinum-based chemotherapy is the conventional chemotherapy regimen for patients with oral squamous cell carcinoma. However, due to the heterogeneity of tumors and individual differences of patients, chemotherapy regimens lacking individualized evaluation of tumor patients are often less effective. Therefore, personalized tumor chemotherapy is one of the effective methods for the future treatment of malignant tumors. The patient-derived xenograft model is a relatively new tumor xenograft model that relies on immunodeficient mice. This model can better maintain various histological characteristics of primary tumor grafts, such as pathological structural features, molecular diversity, and gene expression profiles. Therefore, the patient-derived xenograft model combined with drug screening technology to explore new tumor chemotherapy is the critical research direction for future tumor treatment. This study successfully established the patient-derived xenograft model of oral squamous cell carcinoma. It was verified by hematoxylin-eosin staining and immunohistochemistry that the constructed patient-derived xenograft model retained the pathological and molecular biological characteristics of primary tumors. Our patient-derived xenograft model can be used further to study the oncological characteristics of oral squamous carcinoma and can also be applied to personalize the treatment of oral squamous carcinoma patients, providing a practical resource for screening chemotherapy drugs.

GNIP1 functions both as a scaffold protein and an E3 ubiquitin ligase to regulate autophagy in lung cancer.

BACKGROUND: Glycogen-Interacting Protein 1 (GNIP1), an E3 ligase, is a member of the tripartite motif (TRIM) family proteins. Current studies on GNIP1 mainly focus on glycogen metabolism. However, the function and molecular mechanisms of GNIP1 in regulating autophagy still remains unclear. This study aimed to investigate the regulatory mechanism of GNIP1 in regulating autophagy in non-small cell lung cancer (NSCLC). METHODS: Crystal violet staining assays were used to evaluate the ability of cell growth and proliferation. Transwell and scratch wound healing assays were used to evaluate the cell migration ability. The protein expressions were measured by western blot and immunohistochemistry. Co-immunoprecipitation assays determined the protein-protein interactions. The in vivo effect of GNIP1 on tumor growth was determined by xenograft assay. RESULTS: We found that GNIP1 was overexpressed in tumor tissues and the expression level of GNIP1 was related to the poor prognosis and the survival time of NSCLC patients. In non-small cell lung cancer (NSCLC), GNIP1 increased proliferation and migration of cancer cells by promoting autophagy. Mechanistic studies indicated that GNIP1, as a scaffold protein, recruited BECN1 and LC3B to promote the formation of autophagosomes. Besides, GNIP1 mediated the degradation of 14-3-3ζ, the negative regulator of VPS34 complex, thus promoting autophagy. Overexpressing GNIP1 promoted tumorigenesis and enhanced autophagy in xenograft models. CONCLUSION: GNIP1 promotes proliferation and migration of NSCLC cells through mediating autophagy, which provides theoretical basis for targeting GNIP1 as anti-cancer drugs. Video Abstract.

Retraction notice to: Minimal Scar Dissection for Partial Parotidectomy via a Modified Cosmetic Incision and an Advanced Wound Closure Method [YJOMS 77 (2019) 1317.E1-1317.E9].

This article has been retracted: please see Elsevier Policy on Article Withdrawal (https://www.elsevier.com/about/our-business/policies/article-withdrawal). This article has been retracted at the request of the Editor-in-Chief. The authors have duplicated an image that previously appeared in: J Clin Otorhinolaryngol Head Neck Surg (China) 2018 https://doi.org/10.13201/j.issn.1001-1781.2018.16.011 One of the conditions of submission of a paper for publication is that authors declare explicitly that their work is original and has not appeared in a publication elsewhere. Re-use of any data should be appropriately cited. As such this article represents a severe abuse of the scientific publishing system. The scientific community takes a very strong view on this matter and apologies are offered to readers of JOMS that this was not detected during the submission process.

Dihydroartemisinin Induces ER Stress-Mediated Apoptosis in Human Tongue Squamous Carcinoma by Regulating ROS Production.

BACKGROUND: Tongue squamous cell carcinoma is a fatal disease characterized by high invasion and early metastasis. Dihydroartemisinin, an antimalarial drug with multiple biological activities, is reported to be a potential anti-cancer agent. OBJECTIVE: This study aimed to evaluate the antitumor effect of Dihydroartemisinin on tongue squamous cell carcinoma cells, and to identify the underlying mechanisms of Dihydroartemisinin-induced cell apoptosis. METHODS: Here, Cell Counting Kit 8 assay and colony formation assay were conducted to study cell proliferation. Annexin V-FITC/propidium iodide staining and western blot analysis were performed to analyze cell apoptosis. DCFHDA probe was used to measure the generation of cellular reactive oxygen species. Endoplasmic reticulum stress activation was also determined via western blot analysis. RESULTS: The results showed that Dihydroartemisinin substantially inhibited cell proliferation and induced cell apoptosis in vivo. Moreover, reactive oxygen species production and endoplasmic reticulum stress activation were both observed after stimulation with Dihydroartemisinin. However, the reactive oxygen species inhibitor N-acetylcysteine significantly alleviated Dihydroartemisinin-induced endoplasmic reticulum stress and apoptosis. CONCLUSION: These results imply that Dihydroartemisinin induced cell apoptosis by triggering reactive oxygen speciesmediated endoplasmic reticulum stress in CAL27 cells. In addition, Dihydroartemisinin might be an effective drug for tongue squamous cell carcinoma therapy.

lncRNA SNHG26 promoted the growth, metastasis, and cisplatin resistance of tongue squamous cell carcinoma through PGK1/Akt/mTOR signal pathway.

Tongue squamous cell carcinoma (TSCC) is closely linked to head and neck cancers. Here, we sought to explore the role and mechanism of lncRNAs in the occurrence and progression of TSCC and cisplatin resistance. The results of next-generation transcriptomic sequencing revealed that lncRNA-SNHG26 was differentially expressed and was associated with TSCC cisplatin resistance. The Cancer Genome Atlas dataset and tumor tissue analysis revealed that high SHNG26 expression was associated with the occurrence, progression, and poor prognosis of TSCC. Evidence from cell and animal experiments showed that SNHG26 expression was positively correlated with TSCC proliferation, epithelial-mesenchymal transformation, migration, invasion, and cisplatin resistance. Furthermore, in TSCC cells, SNHG26 was found to bind directly to the PGK1 protein, inhibiting its ubiquitination and activating the Akt/mTOR signaling pathway. These findings suggest that lncRNA-SNHG26 may be a promising target for inhibiting TSCC progression and improving sensitivity to cisplatin chemotherapy in TSCC.

Glaucocalyxin A induces apoptosis and autophagy in tongue squamous cell carcinoma cells by regulating ROS.

PURPOSE: Tongue squamous cell carcinoma (TSCC) is the most common highly invasive oral cancer. Glaucocalyxin A (GLA) is a diterpenoid component isolated from Rabdosia japonica var. with anti-bacterial and anti-cancer biological properties. However, the role of GLA in human TSCC remains uncertain. The aim of this paper was to investigate the anti-cancer effect of GLA on TSCC cells as well as its underlying mechanism. METHODS: Cell viability and growth were analyzed by CCK-8 assay and colony formation, respectively. DAPI staining and flow cytometry assay were used to detect the cell apoptosis. Lysotracker Red staining was used to observe the lysosomes and autolysosomes of TSCC cells. ROS fluorescent probe was used to test the intracellular ROS levels. Western blotting was used to detect the expression levels of apoptosis- and autophagy-related proteins. RESULTS: GLA inhibits the cell viability and growth in TSCC cells. GLA induces TSCC cells apoptosis, autophagy and ROS production in a time- and concentration-dependent manner. In addition, GLA inhibits the viability of TSCC cells by inducing intracellular ROS production. Finally, GLA triggers ROS-dependent apoptosis and autophagy in TSCC cells. CONCLUSION: Our results consistently suggested that GLA can induce apoptosis and autophagy in TSCC cells by generating ROS. GLA may serve as a promising therapeutic drug for overcoming TSCC.

Prognostic significance of an autophagy-related long non-coding RNA signature in patients with oral and oropharyngeal squamous cell carcinoma.

Traditional clinicopathological indices are insufficient in predicting the prognosis of patients diagnosed with oral and oropharyngeal squamous cell carcinoma (OSCC/OPSCC). Notably, autophagy and long non-coding RNAs (lncRNAs) regulate the development and progression of various types of cancer. The present study aimed to assess the association between autophagy-related lncRNAs and the prognosis of patients diagnosed with OSCC/OPSCC. Gene sequencing and clinicopathological data of patients with OSCC/OPSCC were downloaded from The Cancer Genome Atlas database, while gene set functional classification was downloaded from the Gene Set Enrichment Analysis database. Out of the 413 transcriptome data samples and 402 clinicopathological data samples retrieved, a total of nine autophagy-related lncRNAs, including PTCSC2, AC099850.3, LINC01963, RTCA-AS1, AP002884.1, UBAC2-AS1, AL512274.1, MIR600HG and AL354733.3, were screened. This was geared towards establishing a signature through gene co-expression network, univariate and Least Absolute Shrinkage and Selection Operator Cox regression analyses. Based on this signature, the patients were subdivided into a high-risk group and a low-risk group. Kaplan-Meier survival analysis revealed that the overall survival of the high-risk group was significantly lower than that of the low-risk group. Furthermore, principal components analysis demonstrated that the patients diagnosed with OSCC/OPSCC could be distinguished into low-survival and high-survival groups according to the signature. Univariate and multivariate Cox regression analyses of clinicopathological data and the signature revealed that the signature could potentially be used as an independent prognostic factor for OSCC/OPSCC. In addition, reverse transcription-quantitative PCR analysis of clinical samples demonstrated the validity of the signature. In summary, the present study revealed that the signature based on autophagy-related lncRNAs potentially acts as an independent prognostic indicator for patients with OSCC/OPSCC. Furthermore, it promotes research on targeted diagnosis and treatment of patients diagnosed with OSCC/OPSCC.

A competing risk nomogram for predicting cancer-specific death of patients with buccal mucosa cancer.

OBJECTIVES: Our aim was to develop and validate a competing risk nomogram to determine the probability of cancer-specific death in buccal mucosa cancer (BMC) patients. MATERIALS AND METHODS: We examined the records of BMC patients in the Surveillance, Epidemiology, and End Results (SEER) Program and First Affiliated Hospital of Nanchang University (China). We adopted the cumulative incidence function and Fine-Gray proportional hazards model based on univariate and multivariate analyses by R-software to identify the risk factors associated with cancer-specific death. Subsequently, a nomogram was developed and validated to predict the 3- and 5-year probability of cancer-specific death. RESULTS: In 1,286 BMC patients identified from SEER database, cumulative incidences of cancer-specific death after diagnosis were 33.4% and 35.5% for 3 and 5 years, respectively. In the training cohort (n = 902) from SEER database, the Fine-Gray model indicated that age, Tumor Node Metastasis (TNM) stages, grade, surgery, and histological type were independent risk factors associated with cancer-specific death, based on which a prognostic nomogram was developed. In the internal validation cohort from SEER database (n = 384) and the external validation cohort from our medical center (n = 174), the nomogram was well calibrated and showed remarkable prediction performance. CONCLUSION: The nomogram created herein may prove to be a good assistant tool for assessing the prognosis of BMC patients.

Establishment of a Jaw Fibrosarcoma Patient-Derived Xenograft and Evaluation of the Tumor Suppression Efficacy of Plumbagin Against Jaw Fibrosarcoma.

Background: Head and neck fibrosarcoma is a rare malignant tumor, accounting for about 1% of all head and neck tumors. It can also occur in the jaw bone, for which surgical resection is the main treatment but the recurrence rate is high and the prognosis is usually poor. Due to the lack of models mimicking the biological characteristics of the tumor, there is little progress in the research of the pathogenesis and treatment of fibrosarcoma. Therefore, there is an urgent need to explore a high-fidelity model that can reflect the biological characteristics of fibrosarcoma for the sake of improving the therapeutic outcome and prognosis, and preventing recurrence. Patient-derived xenografts (PDX) may more accurately reflect the human disease, and is an attractive platform to study disease biology and develop treatments and biomarkers. In this study we describe the establishment of jaw fibrosarcoma PDX models and compare PDX tumors to those of human origin. Methods: Tumor biopsies from a patient with jaw fibrosarcoma were implanted in immunodeficient mice. Primary and PDX tumors were characterized extensively by histology, immunohistochemistry and humanized identification. Based on the finding of our previous preliminary research that plumbagin had an anti-tumor effect against head and neck cancer, we used this model in the present study to evaluate the anti-tumor effect of plumbagin on jaw fibrosarcoma. Results: The established PDX model maintained the histological and immunohistochemical characteristics of the primary tumor. Plumbagin significantly inhibited the tumor growth in the jaw fibrosarcoma PDX model. Conclusion: We successfully established a PDX model of jaw fibrosarcoma and demonstrated that this PDX model preserved the important molecular characteristics of the human primary tumor, thus providing a powerful tool for treatment research and new drug development of jaw fibrosarcoma. In addition, plumbagin was found to have an inhibitory effect on the growth of PDX modeled jaw fibrosarcoma, which provides a preliminary research basis for its clinical application.

Association between microRNA-125b expression in formalin-fixed paraffin-embedded tumor tissues and prognosis in patients with melanoma.

Melanoma is an invasive and malignant type of tumor with unsatisfactory therapeutic outcomes. The present study aimed to detect the expression levels of microRNA (miR)-125b in formalin-fixed paraffin-embedded (FFPE) melanoma tissues and the association of its expression levels with the clinical features, diagnosis and prognosis of melanoma. Expression levels of miR-125b in 29 FFPE melanoma specimens (16 primary and 13 metastatic tumors), and 16 intradermal nevus (IDN) specimens as a control, were detected by reverse transcription-quantitative PCR. Associations among miR-125b expression and mortality, patient age and sex, tumor location and size, lymph node metastasis (LNM) and TNM stage were analyzed by t-test. The diagnostic value of miR-125b for melanoma was evaluated by receiver operating characteristic (ROC) curve analysis. Prognosis of patients in the microRNA-125b low- and high-expression groups was analyzed by Fisher's exact test. The association between miR-125b expression and the overall survival of patients with melanoma was assessed using Kaplan-Meier curve analysis and a Cox proportional hazards model. The results revealed that the expression levels of miR-125b in primary and metastatic melanomas were significantly lower than those in the IDN control group (P<0.05), and the expression levels of miR-125b in the metastatic group were significantly lower than those in the primary group (P<0.05). In addition, the expression levels of miR-125b were significantly associated with LNM (P=0.001) and TNM stage (P=0.004), but not with age, sex, tumor size or location (P>0.05). ROC curve analysis revealed that the area under the curve (AUC) was 0.880, with a 95% CI of 0.777-0.984 (P<0.05). The overall survival rate of the patients with a low expression level of miR-125b (20.0%) was lower than that of patients with a high expression level of miR-125b (64.3%) (P<0.05). miR-125b expression was an independent predictor of overall survival in patients with melanoma [hazard ratio (HR), 0.252; 95% CI, 0.087-0.729]. Overall, these findings indicated that a low expression level of miR-125b was associated with higher LNM and TNM stage in patients with melanoma, and that this has a certain diagnostic value. miR-125b may be used for the early screening of melanoma and determining the prognosis of patients with melanoma, and may be a potential target for the treatment of the disease.

Inhibition of USP4 attenuates pathological scarring by downregulation of the TGF­ß/Smad signaling pathway.

Pathological scarring is a result of the hypertrophy of scar tissue during tissue repair following trauma. The aim of the present study was to assess the effect of ubiquitin­specific protease 4 (USP4) silencing on pathological scarring, and to evaluate the mechanistic basis for the effect. An MTT assay was used to assess cell viability. Immunoprecipitation (IP) was used to determine ubiquitination levels of the TGF­ß receptor (TßR)I and Smad7. Tumor formation was assessed by injecting keloid fibroblasts. Hematoxylin and eosin staining was used to detect pathological changes in tumor tissue. Reverse transcription quantitative polymerase chain reaction and western blot analysis assays were used to evaluate the expression levels of TßRI and Smad7. Compared with the untreated control animals, cell viability and the expression of TßRI and Smad7 increased significantly in animals treated with TGF­ß. Short hairpin RNA for USP4 (shUSP4) decreased the cell viability of negative control cells, TGF­ß­induced cellular proliferation, and the expression of TßRI and Smad7. IP experiments indicated that the ubiquitination level of TßRI was decreased following USP4 silencing. There was no remarkable difference in the structure of scar tissue among the various animal groups at 14 days following treatment, while the necrotic area of the scar tissue in the shUSP4 and vialinin A (USP inhibitor)­treated animals increased significantly at the 28th and 42nd day compared with the control animals. At days 14, 28 and 42, the expression levels of TßRI and Smad7 in the shUSP4 and vialinin A­treated animals were significantly decreased compared with the control animals (P<0.05). In summary, interference with or inhibition of USP4 prevented the activity of the TGF­ß/Smad pathway signaling and inhibited the formation of pathological scars.

Minimal Scar Dissection for Partial Parotidectomy via a Modified Cosmetic Incision and an Advanced Wound Closure Method.

PURPOSE: To evaluate the usefulness of the modified cosmetic incision (MCI) and advanced wound closure method in partial parotidectomy by comparison with the modified Blair incision (MBI). PATIENTS AND METHODS: This study retrospectively enrolled 44 patients who underwent partial parotidectomy for benign parotid tumors. These patients were divided into 2 groups: MCI group and MBI group. The MCI surgical procedures were performed via a minimal facelift incision with no preauricular incision, postauricular and hairline incision, or extensive hairline incision and an advanced wound closure method, using continuous absorbable intradermal sutures and skin adhesive. The MBI surgical procedures were performed via a conventional MBI and standard transdermal, interrupted, nonabsorbable suturing approach. The operation variables and the cosmetic results of the patients in each group were compared. RESULTS: A total of 23 patients underwent the MCI and advanced wound closure approach and 21 patients underwent the MBI and standard wound closure approach. No significant differences were found in gender, mean age, tumor size, or tumor site between the 2 groups (P > .05). No differences between groups were seen in operative time and intraoperative blood loss volume (P > .05). Several postoperative complications, such as facial paralysis, Frey syndrome, salivary fistula, infection, or tumor recurrence, did not differ between the 2 groups (P > .05). However, postoperative drainage volume in the MCI group was significantly lower than that in the MBI group (P < .01). Moreover, the postoperative cosmetic satisfaction, skin numbness, and scar evaluation results in the MCI group were better than those in the MBI group (P < .001). CONCLUSIONS: MCI combined with continuous absorbable intradermal sutures and skin adhesive for partial parotidectomy is technically feasible and safe and could produce excellent cosmetic outcomes in selected patients with benign parotid tumors.

Cryptotanshinone sensitizes antitumor effect of paclitaxel on tongue squamous cell carcinoma growth by inhibiting the JAK/STAT3 signaling pathway.

Cryptotanshinone, a natural compound isolated from the roots of Salvia miltiorrhiza Bge (Danshen), has been found to induce cancer cells apoptosis and impair cell migration and invasion in various malignancies, but its antiproliferation and chemosensitization effects of Cryptotanshinone on tongue squamous cell carcinoma(TSCC)still remain fully elucidated. In this study, the effects of Cryptotanshinone on the proliferation, apoptosis and cell cycle of human TSCC cells, including CAL 27 and SCC 9 cells, were measured. The results demonstrated that Cryptotanshinone dose-dependently inhibited cell migration and proliferation, and induced apoptosis in TSCC cells. Mechanistic study revealed that Cryptotanshinone suppressed the expression of p-STAT3, Bcl-2, CDK2, Snail and MMP2, and induced the expression of E-cadherin, P53, P21 and ß-catenin. Furthermore, we found that the combination treatment of Cryptotanshinone and paclitaxel more effectively inhibited TSCC cell proliferation and migration, and induced apoptosis via the inhibition of STAT3 signaling pathway. In brief, we provided the new evidence that Cryptotanshinone could enhance the efficacy of paclitaxel on TSCC cells in vitro and demonstrated that STAT3 signaling pathway played an important role in Cryptotanshinone-induced anticancer effects in human TSCC.